You have triglycerides. So do we. Sometimes a lot, sometimes not, sometimes too many. They’re formed by combining glycerol with three molecules of fatty acid, which can be the same or different. Glycerol is a sugar alcohol that provides the backbone of many lipids. It’s an important intermediate in carbohydrate and fat metabolism. High levels of triglycerides have been linked to atherosclerosis and heart disease. They’re the natural molecular form that makes up virtually all fats and oils in both plants and animals. Most of us know our cholesterol levels, and we even know about the differences between HDL and LDL. But managing triglycerides (TG’s) is just as important to cardiac health. About a third of U.S. adults have borderline TG levels, between 150 and 199 milligrams per deciliter. Many of those with high TG’s are older whites who smoke, are overweight, and who get less than 150 minutes of exercise a week. Women have a lower risk than men, and blacks and Mexican Americans have even lower risks (Ford, 2009).

The body makes TG’s from carbohydrates and sends them to fat cells where they’re stored for energy. High TG levels often accompany low HDL, in a kind of lipid profile that may run in families. HDL cholesterol between 40 and 60 milligrams per deciliter, and LDL less than 100 are reasonable goals. Where TG’s store unused calories and provide energy, cholesterol is used to build cells and to make some hormones. Really high TG’s can be a sign that something else is amiss, like high blood pressure or high blood glucose. Low thyroid hormones, liver or kidney conditions, and some genetic missteps can affect how the body converts fat to energy, so TG readings will be elevated. But beta blockers taken for high blood pressure, some diuretics, steroids and birth control pills can raise TG levels, too.

Lifestyle changes are the first line of defense against high TG’s. Losing weight, cutting calories and avoiding excess sugars and refined foods are simple steps, although weight loss may initially be a challenge. It takes only a few pounds to make a difference, and light exercise and alcohol avoidance can help. But there is a supplement that can rescue high TG’s—fish oil. Of course, when Big Pharma realized this, they had to make a prescription form—Lovaza, Glaxo Smith-Kline’s omega-3 prescription. What makes it different from plain fish oil is the FDA’s blessing, which states that Lovaza is the only omega-3 medication so approved. No other fish oil product may be called a medication. The same effect, though, can be realized by taking multiple capsules of OTC product. But because one’s prescription plan pays for Lovaza, it’s cheaper for the patient…and GSK makes a ton of money.

Fish oil contains EPA and DHA, fatty acids that benefit the cardiovascular system and the eyes and brain, respectively. The fatty acids from fish oils are anti-inflammatory and anti-thrombotic; they compete successfully with substances that cause platelet aggregation and vasoconstriction. In hypertriglyceridemia, fish oil decreases the secretion of very low density lipoproteins (VLDL), increases VLDL clearance and reduces TG transport (Nestel, 2000) (Stark, 2000). It is held that fish oil can influence CVD risk factors to such an extent as to reduce risk of coronary heart disease by as much as twenty-seven percent (Stark, 2000).

Some products labeled as fish oil are not really oils at all, but rather alternate lipids known as fatty acid ethyl esters, differing from authentic fish oil triglycerides. Because free fatty acids are rapidly oxidized, the TG structure offers greater stability to the fatty acids and prevents breakdown and oxidation (Segura, 1988). Ethyl esters are derived from the reaction of free fatty acids with ethanol. Here, the glycerol backbone of the TG is removed and substituted with alcohol (Mogelson, 1984). The resulting ester allows for fractional distillation of the long-chain fatty acids at lower temperatures. At this point, the EPA and DHA can be manipulated to levels greater than those found in the fish (Saghir, 1997). Ethyl esters (EE’s) are uncommon in nature, so are not properly digested and absorbed by the body. The process can be reversed by using food grade enzymes, restoring the product to its rightful TG form with the glycerol backbone. Doing this is not common to the industry because of the cost. The fatty acid-ethanol bond is about fifty times more resistant to digestive enzymes (pancreatic lipase) as compared to the triglyceride form (Yang, 1990) (Yang, 1990). TG fish oil yields fifty percent more plasma EPA/DHA after absorption than the EE form (Beckerman, 1990) (Dyerberg, 2010). Over the long term, however, EE absorption seems to equal out after a few months’ intake (Sadovsky, 2009). It is conjectured that the slower activity of EE fish oil results in sustained inhibition of sodium and calcium channels, helping to prevent arrhythmia (Leaf, 2003) (Lavie, 2009).

There is no discernible health risk to EE fish oil, not even for a person sensitiveto alcohol. There are stories about EE being able to melt polystyrene. Alcoholand water are polar substances, having different electrical charges at oppositeends. They do not react with non-polar materials, such as Styrofoam. So, if you’veever heard that EE fish oil will dissolve a Styrofoam cup, dismiss the thought.When it comes to oxidation, though, EE will oxidize faster than the TG fish oil,making it less reliable (Song, 1997). The TG fish oil is naturally occurringand less likely to go rancid. Doubtless there are myriad studies to support andnegate the efficacy of each form, but if either one lowers your triglyceridelevels, there’s no debate.